Smoking and the development of atherosclerosis
- The effects of smoking on endothelial cells.
- The effects of smoking on plasma lipoproteins.
- The effects of smoking on platelet function.
- The effects of smoking on white blood cells.
Pharmacology of nicotine
- Mechanisms of action.
Michael Pittilo R. Cigarette smoking, endothelial injury and cardiovascular disease. Int J Exp Pathol 2000;81:219-230.
This review concentrates on new evidence regarding the precise components of cigarette smoke responsible for the relationship between cigarette smoking and cardiovascular disease as well as the mechanisms by which they exert their effect.
Villablanca AC, McDonald JM, Rutledge JC. Smoking and cardiovascular disease. Clin Chest Med 2000;21:159-172.
The relationships between smoking and cardiovascular disease result from multiple mechanisms that interact to contribute to atherosclerosis, vascular injury, thrombosis, and vascular dysfunction. This article reviews our current understanding of how smoking contributes to the genesis and progression of these disorders.
Powell JT. Vascular damage from smoking: disease mechanisms at the arterial wall. Vasc Med 1998;3:21-28.
This article reviews the mechanisms of arterial wall damage caused by smoking. Several products of tobacco combustion, including nicotine, free radicals and aromatic compounds, have been shown to cause release of catecholamines, endothelial injury, oxidation of LDL, increase of plasma fibrinogen and alteration of platelet activity. All these proatherogenic effects of smoking are summarized in this paper.
Benowitz NL. The role of nicotine in smoking-related cardiovascular disease. Prev Med 1997;26:412-417.
This article review current evidence showing that nicotine contributes, via its hemodynamic effects, to acute cardiovascular events. However, the effects of nicotine are much less important than are the prothrombotic effects of other products of tobacco combustion. Another issue that is emphasized is that the dose response for cardiovascular events of nicotine appears to be flat, suggesting that if nicotine is involved, adverse effects might be seen with relatively low-level cigarette exposures.
Krupski WC. The peripheral vascular consequences of smoking. Ann Vasc Surg 1991;5:291-304.
Nicotine and carbon monoxide produce acute cardiovascular consequences, including altered myocardial performance, tachycardia, hypertension, and vasoconstriction. Smoking injures blood vessel walls by damaging endothelial cells, thus increasing permeability to lipids and other blood components. Among metabolic and biochemical changes induced by smoking are a tendency for increased serum cholesterol, reduced high density lipoprotein, elevated plasma free fatty acids, elevated vasopressin, and a thrombogenic balance of prostacyclin and thromboxane A2. In addition to rheologic and hematologic changes from increased erythrocytes, leukocytes, and fibrinogen, smokers have alterations in platelet aggregation and survival that produce thrombosis. All of these interactive mechanisms by which smoking exerts its deleterious effects are summarized in this article.
Posted June 2010